We are attempting to delineate the mechanisms whereby acute tissue injury leads to elevation of C-reactive protein concentrations in sera. We have learned thus far that this increase is a result of acceleration in rate of synthesis of this protein by the liver. This, in turn, results from a gradual increase in the number of cells making CRP; this increase seem to result from recruitment to CRP formation of cells not previously making this protein. We are now investigating whether circulating plasma factors, cellular elements or neurogenic mechanisms cause this recruitment. We are exploring the role of the RE system in the CRP response and are trying to demonstrate mediator activity in in vitro systems.